Sleep & breathing = Schlaf & Atmung · 2013
Endothelial injury markers before and after nasal continuous positive airway pressure treatment for obstructive sleep apnoea hypopnoea syndrome.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
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Wilczynska Maria, Rice Samuel, Davies Gareth, Lewis Keir E
Аннотация
PURPOSE: The purpose of this study was to evaluate whether serum amyloid A (SAA), C-reactive protein (CRP), vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) levels are elevated in obstructive sleep apnoea hypopnoea syndrome (OSAHS), and whether they change following acute- and medium-term CPAP treatment.
METHODS: Consecutive subjects (n = 40) referred to the Sleep Disordered Breathing Unit were included in the research. Sera were sampled in the afternoon prior to an in-hospital limited-channel sleep study and on the next morning. Those diagnosed with OSAHS were commenced on CPAP and had further blood samples collected in the morning after the first night and then after a month of treatment.
RESULTS: We had 20 subjects with moderate/severe OSAHS (mean ± SD), 4% desaturation rate (4% DR) 44.3 ± 31.4 events/h, and 20 comparator subjects with symptoms but negative sleep studies, 4% DR 5.6 ± 2.9 events/h. There was no difference in the morning and afternoon vascular injury marker levels between the OSAHS and comparator groups. However, CRP (6.52 ± 9.53 vs. 5.58 ± 8.47, p = 0.04) and VCAM-1 (366.30 ± 90.11 vs. 339.60 ± 95.87, p = 0.02) levels showed significant diurnal variation within the OSAHS group with higher afternoon levels compared to morning measurements. There were no changes in any of the vascular injury marker levels following CPAP.
CONCLUSIONS: This study demonstrates that OSAHS leads to endothelial dysfunction as reflected by higher afternoon than morning CRP and VCAM-1 levels. However, despite a good CPAP compliance, a month of treatment does not decrease vascular injury marker levels.
METHODS: Consecutive subjects (n = 40) referred to the Sleep Disordered Breathing Unit were included in the research. Sera were sampled in the afternoon prior to an in-hospital limited-channel sleep study and on the next morning. Those diagnosed with OSAHS were commenced on CPAP and had further blood samples collected in the morning after the first night and then after a month of treatment.
RESULTS: We had 20 subjects with moderate/severe OSAHS (mean ± SD), 4% desaturation rate (4% DR) 44.3 ± 31.4 events/h, and 20 comparator subjects with symptoms but negative sleep studies, 4% DR 5.6 ± 2.9 events/h. There was no difference in the morning and afternoon vascular injury marker levels between the OSAHS and comparator groups. However, CRP (6.52 ± 9.53 vs. 5.58 ± 8.47, p = 0.04) and VCAM-1 (366.30 ± 90.11 vs. 339.60 ± 95.87, p = 0.02) levels showed significant diurnal variation within the OSAHS group with higher afternoon levels compared to morning measurements. There were no changes in any of the vascular injury marker levels following CPAP.
CONCLUSIONS: This study demonstrates that OSAHS leads to endothelial dysfunction as reflected by higher afternoon than morning CRP and VCAM-1 levels. However, despite a good CPAP compliance, a month of treatment does not decrease vascular injury marker levels.